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慢速骨骼肌肌钙蛋白 T 基因在发育中和患病的人心肌中表达。

The slow skeletal muscle troponin T gene is expressed in developing and diseased human heart.

机构信息

National Heart and Lung Institute, Imperial College, London, Heart Science Centre, Harefield, Middlesex, UB9 6JH, UK.

Department of Basic Sciences, Royal Veterinary College, Royal College Street, London, NW1 0TU, UK.

出版信息

Mol Cell Biochem. 2004 Aug;263(1):91-7. doi: 10.1023/B:MCBI.0000041851.53074.72.

DOI:10.1023/B:MCBI.0000041851.53074.72
PMID:27520668
Abstract

Cardiac muscle development is characterised by the activation of contractile protein genes and subsequent modulation of expression resulting, ultimately, in the formation of a mature four-chambered organ. Myocardial gene expression is also altered in the adult in response to pathological stimuli and this is thought to contribute to the altered contractile characteristics of the diseased heart. We have examined the expression of the slow skeletal troponin T (TnT) gene in the human heart during development and in disease using whole mount in situ hybridisation and real-time quantitative (TaqMan) polymerase chain reaction (PCR). Slow skeletal TnT mRNA shows transitory and regional expression in the early foetal heart, which occurs at different times in atria and ventricles. In ventricular myocardium, expression is seen in the outer epicardial layer at a time when the coronary circulation is being established. Expression was detected at low levels in the adult human heart and was significantly increased in end-stage heart failure. Similarly, expression was readily detectable during early rat heart development and was up-regulated in pressure overload hypertrophy in adult. Together these data show for the first time that slow skeletal TnT mRNA is readily detectable during early human heart development. They further suggest that slow skeletal TnT may be responsive to myocardial stress and that elevated levels may contribute to myocardial dysfunction in adult disease. (Mol Cell Biochem 263: 91-97, 2004).

摘要

心肌发育的特征是收缩蛋白基因的激活,以及随后表达的调节,最终导致成熟的四腔器官的形成。心肌基因表达在成年期也会因病理刺激而改变,这被认为是导致病变心脏收缩特性改变的原因。我们使用整体原位杂交和实时定量(TaqMan)聚合酶链反应(PCR)检测了人类心脏在发育过程中和疾病中的慢骨骼肌肌钙蛋白 T(TnT)基因的表达。慢骨骼肌 TnT mRNA 在早期胎儿心脏中表现出短暂和区域表达,在心房和心室中发生的时间不同。在心室心肌中,在冠状动脉循环建立时,可以在外胚层看到表达。在成年人心肌中以低水平检测到表达,在终末期心力衰竭中显著增加。同样,在大鼠心脏早期发育过程中很容易检测到表达,并在成年压力超负荷肥大中上调。这些数据首次表明,慢骨骼肌 TnT mRNA 在人类心脏早期发育过程中很容易检测到。它们进一步表明,慢骨骼肌 TnT 可能对心肌应激有反应,并且高水平可能导致成年疾病中的心肌功能障碍。(分子细胞生化 263: 91-97, 2004)。

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